Anti-apoptotic effect of quercetin: intervention in the JNK- and ERK-mediated apoptotic pathways.

@article{Ishikawa2000AntiapoptoticEO,
  title={Anti-apoptotic effect of quercetin: intervention in the JNK- and ERK-mediated apoptotic pathways.},
  author={Yoshihisa Ishikawa and Masanori Kitamura},
  journal={Kidney international},
  year={2000},
  volume={58 3},
  pages={
          1078-87
        }
}
BACKGROUND Bioflavonoid quercetin inhibits hydrogen peroxide (H2O2)-induced apoptosis via intervention in the activator protein 1 (AP-1)-mediated apoptotic pathway. In this report, we investigated molecular events involved in the anti-apoptotic effect of quercetin, focusing especially on its effects on the family of mitogen-activated protein (MAP) kinases. METHODS Cultured mesangial cells were exposed to H2O2, and activation of c-Jun N-terminal kinase (JNK), extracellular signal-regulated… 

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References

SHOWING 1-10 OF 46 REFERENCES

Unexpected protection of glomerular mesangial cells from oxidant-triggered apoptosis by bioflavonoid quercetin.

The novel action of quercetin as an apoptosis inhibitor was found to be via suppression of the tyrosine kinase-c-Jun/AP-1 pathway triggered by oxidant stress.

Opposing Effects of ERK and JNK-p38 MAP Kinases on Apoptosis

The effects of dominant-interfering or constitutively activated forms of various components of the JNK-p38 and ERK signaling pathways demonstrated that activation of JNK and p38 and concurrent inhibition of ERK are critical for induction of apoptosis in these cells.

Role of extracellular signal-regulated protein kinases in apoptosis by asbestos and H2O2.

It is demonstrated in rat pleural mesothelial cells that apoptotic concentrations of crocidolite asbestos and H2O2 induce phosphorylation and activation of extracellular signal-regulated protein kinases (ERK), suggesting that distinct cell-signaling cascades may be important in phenotypic responses elicited by oxidant stresses.

Inhibition of the c-Jun N-terminal kinase (JNK) signaling pathway by curcumin

The inhibition of the MEKK1-JNK pathway reveals a possible mechanism of suppression of AP-1 and NF-κB signaling by curcumin, and may explain the potent anti-inflammatory and anti-carcinogenic effects of this chemical.

Induction of Apoptosis by ASK1, a Mammalian MAPKKK That Activates SAPK/JNK and p38 Signaling Pathways

Overexpression of ASK1 induced apoptotic cell death, andASK1 was activated in cells treated with tumor necrosis factor-α, and TNF-α-induced apoptosis was inhibited by a catalytically inactive form of AsK1.

The cellular response to oxidative stress: influences of mitogen-activated protein kinase signalling pathways on cell survival.

The results suggest that ERK and JNK/SAPK act in opposition to influence cell survival in response to oxidative stress, whereas neither p38 nor NF-kappaB affects the outcome.

Mitogen-activated protein kinase-mediated Fas apoptotic signaling pathway.

Data indicate that the ERK and the JNK groups of MAP kinases cooperate in the induction of cell death by Fas, and that both JNK and ERK protein kinases were activated upon Fas crosslinking through a Ras-dependent mechanism.

Activation of Stress Signaling Pathways by the End Product of Lipid Peroxidation

The findings that HNE strongly induced intracellular peroxide production, HNE-induced JNK activation was inhibited by pretreatment of the cells with a thiol antioxidant, N-acetylcysteine, and H2O2 significantly activated JNK support the hypothesis that pro-oxidants play a crucial role in the H NE-induced activation of stress signaling pathways.

Extracellular signal-regulated kinase (ERK) activity is required for TPA-mediated inhibition of drug-induced apoptosis.

It is concluded that TPA inhibits the induction of apoptosis in anisomycin-treated HL-60 cells through an ERK-dependent pathway and that this effect can be reversed by the attenuation of ERK activity accompanied with the stimulation of JNK/SAPK activity.

Oxidant stress incites spreading of macrophages via extracellular signal-regulated kinases and p38 mitogen-activated protein kinase.

Results suggest that oxygen radical metabolites, the well-known mediators for tissue injury, incite spreading of macrophages via the MAP kinase-SRE signaling pathways.